Full Profile

After graduating from the University of Salford in 2003 with a BSc (Hons.) in Biochemistry, Vicky moved to the University of Manchester where she completed her PhD under the supervision of Prof. Alex Verkhratsky and Dr. Owen Jones. Her thesis, entitled “continuity in the neuronal endoplasmic reticulum”, focused on the development of two new lentivirally-delivered fluorescent reporters to visualise the endoplasmic reticulum (ER) in cultured neurons and in brain slices. Using these reporters Vicky provided the first direct evidence of a single, continuous ER lumen extending throughout the cell both in neurons and in astrocytes.

Vicky remained at the University of Manchester and undertook two postdoctoral research positions. The first built upon her PhD work, exploiting the newly developed fluorescent reporters to investigate the morphology and integrity ER in Alzheimer’s disease.

In her second postdoctoral position, Vicky joined the lab of Prof. Philip Woodman to investigate the role of accessory proteins in cargo sorting and intraluminal vesicle formation in the mammalian endocytic pathway.

Vicky took up her current position as lecturer in molecular biology at UCLan in 2011. Her research remains focussed on the cellular causes of neurodegenerative disorders, and Vicky is especially interested in the dysfunction of astrocytes associated with Alzheimer’s disease.

Research

Vicky’s research aims to uncover the subcellular mechanisms which govern the onset and progression of dementias, such as Alzheimer’s disease (AD). Specifically, Vicky is interested in exploring the calcium hypothesis of AD; the theory that disruption in intracellular calcium levels either triggers or worsens the brain cell death seen in this disease.

Much of the research conducted to date has focussed on calcium dysregulation in neurons, as it is these crucial impulse-carrying cells which die off in brain areas crucial for learning and memory. However, it is now known that neurons are not the only type of cell in the brain that is affected by AD, especially with regards to calcium homeostasis.

Part of the glial family of brain cells, astrocytes were long thought to be relatively quiescent cells; functioning only to nourish and support the neurons. In the last 20 years however their crucial role as subtle modulators of brain activity has emerged. For example, it has been shown that astrocytes envelop some synapses (junctions between neighbouring neurons) and can absorb or release chemicals which alter the transmission of information between the neurons.

Like other cells, calcium serves as an extremely important messenger in astrocytes. Through the action of the endoplasmic reticulum (ER; a large organelle extending throughout the cell), astrocytes can pass signals around the cell and even to neighbouring cells by carefully releasing stored calcium. This acts as an important communication mechanism that permits messages about brain activity in one region to be passed through a network of connected astrocytes to bring about changes in synapse function.

We now know that calcium handling in astrocytes is disturbed in Alzheimer’s disease, and we also know that this disturbance occurs long before any clinical symptoms of dementia are seen.

Vicky’s research is centred on finding out how Alzheimer’s affects astrocyte structure and function, and how this alteration in functioning may be implicated in the progression of the disease.

To this end, Vicky’s lab is currently investigating how mutant β-amyloid and presenilins (defective proteins associated with familial AD) affect the integrity of the astrocyte ER and the cell’s ability to protect against cell death. She is also working on the development of a new cell line of AD which can be grown easily in the lab to permit quick, inexpensive experiments.